基于解析振速的ESPRIT算法

基于声矢量传感器在二维平面波入射时的输出信息,提出了其"解析振速"的输出模型,将目标的方位信息蕴含在输出信号的相位之中,并由此得到了矢量阵的输出模型.当ESPRIT算法应用于矢量阵时,由于矢量阵的内禀属性,旋转矩阵不再与阵型和信号的频率有关,只与目标方位信息有关,从而能够实现任意阵型全空间的无模糊测向.理论分析和仿真表明:本算法无需先验已知阵型;单声矢量传感器也可以应用ESPRIT算法,且此时其性能逼近克拉美-罗界.湖试表明本算法是有效的.     

单点公交优先感应控制策略效益分析与仿真验证

单点交叉口信号优先可以降低公交车辆延误且易于实现.研究了公交相位绿灯延长、红灯早断和插入相位三种单点公交优先感应控制策略;应用延误三角形方法建立了以公交车辆车均延误变化量和非优先相位车均延误变化量为指标的三种单点公交优先策略效益计算模型.以两相位信号控制为对象,计算对比分析了三种公交优先策略的正负效益及其影响因素,并通过仿真进行了验证分析.研究表明:公交相位绿灯延长、公交相位红灯早断和插入公交相位三种策略都能够降低公交车均延误,与此同时也都会带来非优先相位车流延误的增加,但影响的程度不同.公交相位绿灯延长策略的效益略小于公交相位红灯早断策略,而相位插入策略的效益与插入时刻等多因素相关.     

Regulation of phagocyte migration and recruitment by Src-family kinases

Src-family kinases (SFKs) regulate different granulocyte and monocyte/macrophage responses. Accumulating evidence suggests that members of this family are implicated in signal transduction pathways regulating phagocytic cell migration and recruitment into inflammatory sites. Macrophages with a genetic deficiency of SFKs display marked alterations in cytoskeleton dynamics, polarization and migration. This same phenotype is found in cells with either a lack of SFK substrates and/or interacting proteins such as Pyk2/FAK, c-Cbl and p190RhoGAP. Notably, SFKs and their downstream targets also regulate monocyte recruitment into inflammatory sites. Depending on the type of assay used, neutrophil migration in vitro may be either dependent on or independent of SFKs. Also neutrophil recruitment in in vivo models of inflammation may be regulated differently by SFKs depending on the tissue involved. In this review we will discuss possible mechanisms by which SFKs may regulate phagocytic cell migratory abilities.     

Dissection of a novel molecular determinant mediating Golgi to trans-Golgi network transition

Two major functions of the Golgi apparatus (GA) are formation of complex glycans and sorting of proteins destined for various subcellular compartments or secretion. To fulfill these tasks proper localization of the accessory proteins within the different sub-compartments of the GA is crucial. Here we investigate structural determinants mediating transition of the two glycosyltransferases β-1,4- galactosyltransferase 1 (gal-T1) and the α-1,3-fucosyltransferase 6 (fuc-T6) from the trans-Golgi cisterna to the trans-Golgi network (TGN). Upon treatment with the ionophore monensin both glycosyltransferases are found in TGN-derived swollen vesicles, as determined by confocal fluorescence microscopy and density gradient fractionation. Both enzymes carry a signal consisting of the amino acids E₅P₆ in gal-T1 and D₂P₃ in fuc-T6 necessary for the transition of these glycosyltransferases from the trans-Golgi cisterna to the TGN, but not for their steady state localization in the trans-Golgi cisterna. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. Received 30 July 2008; received after revision 17 September 2008; accepted 29 September 2008     

高频雷达中LFMCW信号的分析

高频雷达在现代战争和民用事业上发挥着越来越重要的作用 ,线性调频连续波 ( L FMCW)信号是高频雷达常采用的信号形式。就 L FMCW信号在高频雷达中的应用作了具体分析 ,并导出了其差频相位的具体表达式 ,它表现出了要检测的各量的物理意义 ,对检测的方法提供了理论依据。在此基础上 ,利用二维 FFT处理技术对目标回波信号的信息提取进行了仿真 ,并对仿真结果进行了分析     

Family I.3 lipase: bacterial lipases secreted by the type I secretion system

Based on the classification of bacterial lipolytic enzymes, family I.3 lipase is a member of the large group of Gram-negative bacterial true lipases. This lipase family is distinguished from other families not only by the amino acid sequence, but also by the secretion mechanism. Lipases of family I.3 are secreted via the well-known type I secretion system. Like most of proteins secreted via this system, family I.3 lipases are composed of two domains with distinct yet related functions. Recent years have seen an increasing amount of research on this lipase family, in terms of isolation, secretion mechanism, as well as biochemical and biophysical studies. This review describes our current knowledge on the structure-function relationships of family I.3 lipase, with an emphasis on its secretion mechanism. Received 18 April 2006; received after revision 3 July 2006; accepted 24 August 2006     

Lipid-lowering drugs

Although a change in life-style is often the method of first choice for lipid lowering, lipid-lowering drugs, in general, help to control elevated levels of different forms of lipids in patients with hyperlipidemia. While one group of drugs, statins, lowers cholesterol, the other group, fibrates, is known to take care of fatty acids and triglycerides. In addition, other drugs, such as ezetimibe, colesevelam, torcetrapib, avasimibe, implitapide, and niacin are also being considered to manage hyperlipidemia. As lipids are very critical for cardiovascular diseases, these drugs reduce fatal and nonfatal cardiovascular abnormalities in the general population. However, a number of recent studies indicate that apart from their lipidlowering activities, statins and fibrates exhibit multiple functions to modulate intracellular signaling pathways, inhibit inflammation, suppress the production of reactive oxygen species, and modulate T cell activity. Therefore, nowadays, these drugs are being considered as possible therapeutics for several forms of human disorders including cancer, autoimmunity, inflammation, and neurodegeneration. Here I discuss these applications in the light of newly discovered modes of action of these drugs. Received 5 September 2005; received after revision 29 December 2005; accepted 26 January 2006     

Huntington’s disease: from huntingtin function and dysfunction to therapeutic strategies

Huntington’s disease (HD) is a neurodegenerative disorder that usually starts in middle age and is characterized by involuntary movements (chorea), personality changes and dementia, leading to death within 10–20 years. The defective gene in HD contains a trinucleotide CAG repeat expansion within its coding region that expresses a polyglutamine repeat in the protein huntingtin. Together with the characteristic formation of aggregates in HD, aberrant protein interactions and several post-translational modifications affect huntingtin during disease progression and lead to the dysfunction and death of selective neurons in the brains of patients. The exact molecular mechanisms by which mutant huntingtin induces cell death are not completely understood but may involve the gain of new toxic functions and the loss of the beneficial properties of huntingtin. This review focuses on the cellular functions in which huntingtin is involved and how a better understanding of pathogenic pathways can lead to new therapeutic approaches. Received 24 May 2006; received after revision 5 July 2006; accepted 23 August 2006     

公交优先的信号控制策略研究

研究了公交优先信号控制策略,模拟路边建立公交车辆检测器的情况下,不同交通流量和公交车发车间隔的最优控制策略,研究发现：当交通流量小于300辆／h．车道时,公交优先信号控制策略能显著地减少乘客的延误时间,而当交通流量达到500辆／h．车道时,即使有公交优先控制策略,而无公交专用道路,也不能有效减少乘客的延误时间,模拟实验的结果是：找到了使公交优先信号控制有效的交通流量和公交车发车间隔的阈值。     

高动态GPS/INS组合导航算法研究

首先介绍了新型深组合GPS/INS系统原理图及组合导航滤波算法。在该算法中,组合卡尔曼滤波器除完成INS误差及GPS接收机时钟误差的估计外,还参与了GPS码跟踪,即完成传统码跟踪环中环路滤波器的功能。采用自适应码跟踪误差估计器补偿组合卡尔曼滤波器测量值中的相关分量,从而消除了传统组合中不稳定的主要根源。然后进行了计算机仿真计算,仿真结果表明,新型深组合GPS/INS导航算法适用于机动性较高的载体。